Nav Beta 3 (SCN3B) belongs to the voltage-gated sodium channel group, and modulates channel gating kinetics. It inactivates the sodium channel opening more slowly than its Beta1 subunit. It is also unique in causing persistent sodium currents which are thought to amplify summation of synaptic imputs which is likely to increase the excitability of specific neurons to their individual inputs (2). Its association with neurofascin may target the sodium channels to the nodes of Ranvier of developing axons and retain these channels at the nodes in mature myelinated axons (1, 2). Defects in SCN3B are the cause of Brugada syndrome (3).
